MMAF

Molecular mechanisms of autophagosome formation

 Coordinatore UNIVERSITAT WIEN 

Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.

 Nazionalità Coordinatore Austria [AT]
 Totale costo 1˙163˙832 €
 EC contributo 1˙163˙832 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2010-StG_20091118
 Funding Scheme ERC-SG
 Anno di inizio 2011
 Periodo (anno-mese-giorno) 2011-03-01   -   2016-02-29

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITAT WIEN

 Organization address address: UNIVERSITATSRING 1
city: WIEN
postcode: 1010

contact info
Titolo: Dr.
Nome: Helmut
Cognome: Schaschl
Email: send email
Telefono: 431428000000
Fax: 43142779172

AT (WIEN) hostInstitution 1˙163˙832.00
2    UNIVERSITAT WIEN

 Organization address address: UNIVERSITATSRING 1
city: WIEN
postcode: 1010

contact info
Titolo: Dr.
Nome: Sascha
Cognome: Martens
Email: send email
Telefono: 431428000000
Fax: 43142779616

AT (WIEN) hostInstitution 1˙163˙832.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

vitro    fuse    cup    small    subunits    bound       membrane    micro    pi    protein    domain    give    structure    shape    double    atg    autophagy    structures    cells    conjugation    autophagosomes    individual    autophagosome   

 Obiettivo del progetto (Objective)

'During autophagy initially small double membrane-bound structures expand and adopt cup-like shapes. These cup-shaped structures fuse at their rims to give rise to autophagosomes within which cytoplasmic material is enclosed. Subsequently autophagosomes fuse with endosomes and lysosomes and the content and the inner membrane are degraded. Autophagy serves to recycle essential building blocks during starvation, to degrade damaged organelles, to clear cells of protein aggregates and to kill intracellular microorganisms. Little is known about the mechanisms by which cells bend and remodel membranes into autophagosomes. The action of a complex containing type III PI3K activity is essential for the initiation of autophagosome formation. During expansion of the initial double membrane bound structure the Atg8 and Atg12 conjugation systems play important roles. A further protein that is essential for autophagosome formation is the transmembrane protein Atg9. We will investigate the impact of individual PI3K complex subunits, the Atg8 and Atg12 conjugation systems and Atg9 on membrane morphology in vitro. We will analyse membrane shape changes and micro-domain formation using artificial small and giant liposomes by electron and light microscopy. We will introduce targeted mutations that are designed to interfere with membrane shape changes or micro-domain formation. Furthermore, where necessary, we will solve the structure of individual subunits or complexes by x-ray crystallography. We will further verify our in vitro findings in cell culture systems. Our results will give important insights into autophagy and organelle formation in general.'

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